FOXO3 and myocardial infarction: Up‐regulated GAS5 expression inhibited cardiomyocyte hypertrophy through negatively regulating miR‐23a and its target forkhead box O3 (Foxo3a).25 Additionally, a previous study confirmed that myocardial infarction‐associated transcript (MIAT) possessed binding sites for miR‐150 and could serve as a miR‐150 sponge in modulating cell proliferation, apoptosis and migration.26 In cultured H9C2 cells, the overexpression of MIAT triggered an Ang II‐induced hypertrophic response via inhibiting the level of miR‐150 level; however, the possible target of miR‐150 was not identified in this study.27